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-<p><strong>Human brain expression data</strong> in patients with Alzheimer&#39;s disease and age-matched elderly control subjects. This cortical expression data set is taken from <a class="fs14" href="http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5281" target="_empty">GEO GSE5281</a> (<a class="fs14" href="http://physiolgenomics.physiology.org/cgi/reprint/28/3/311" target="_empty">Liang et al. 2006</a>, <a class="fs14" href="http://www.pnas.org/lookup/pmid?view=long&amp;pmid=18332434" target="_empty">Liang et al. 2008</a>). Samples were laser-captured from cortical regions of 16 normal elderly humans (10 males and 4 females) and from 33 AD cases (15 males and 18 females). Mean age of cases and controls was 80 years. All samples were run on the Affymetrix U133 Plus 2.0 array. We renormalized the RMA data to an average expression of 8 units on a log2 scale. Two versions of the data have been entered in GeneNetwork: one consisting of 157 of 161 arrays (full set minus 4 arrays we consider of poor quality); the second consisting of what we regard as the best 102 arrays (those with mean correlations of better than 0.88 with all other arrays). Case IDs have the following code structure: Brain Region, GEO ID, Sex, Age, Disease Status. E119615M63N is a sample of the entorhinal cortex of case GSM119615, a male 63 year old normal case. The tissue codes are E = enorhinal cortex layer II, H = hippocampus CA1 pyramidal layer, MT = medial temporal cortex layer III, PC = porterior cingulate cortex layer III, SP = supeior frontal cortex layer III, V = primary visual cortex area 17 layer III. GeneNetwork does not yet allow sophisticated display of the data, but you can perform correlation analyses of any of the 56,000 probe sets. For example, expression of the <em>APP</em> transcript is higher in the AD cases and correlates well with many other AD related genes.</p>
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-<p>NOTE: We detected a minimum of 7.6% case assignment error rate (12 of 158 arrays) in this data set. Twelve cases are assigned to the wrong sex (see <em>XIST</em> probe set 224588_at, the figure below, and table 1). This raises the possibility that some cases are also misassigned by cortical brain region and disease status.</p>
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-<p>&nbsp;</p>
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-<p><img src="http://www.genenetwork.org/images/upload/Xist_in_GSE5281.gif" style="height:250px; width:997px" /></p>
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-<p><small><strong>Legend: </strong>Expression of the sex-specific gene <em>XIST</em> reveals about 10 sex assignment errors in this data set.</small></p>
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-<p>Samples were laser-captured from cortical layer 3 (except the hippocampus) and run on the Affymetrix U133 Plus 2.0 array. We renormalized the data to an average expression of 8 units on a log2 scale. Case IDs have the following code structure: Brain Region, GEO ID, Sex, Age, Disease Status. E119615M63N is a sample of the entorhinal cortex of case GSM119615, a male 63 year old normal case. The tissue codes are E = enorhinal cortex layer II, H = hippocampus CA1 pyramidal layer, MT = medial temporal cortex layer III, PC = porterior cingulate cortex layer III, SP = supeior frontal cortex layer III, V = primary visual cortex layer III. A total of 16 normal subjects were used (10 M and 4 female). The AD samples. GeneNetwork does not allow sophisticated display of the data, but you can perform correlation analyses of any of the 56,000 probe sets. For example expression of the <em>APP</em> transcript is higher in the AD cases and correlates well with many other AD related genes.</p>
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-<p>Information about the genes that are preferentially expressed during the course of Alzheimer&#39;s disease (AD) could improve our understanding of the molecular mechanisms involved in the pathogenesis of this common cause of cognitive impairment in older persons, provide new opportunities in the diagnosis, early detection, and tracking of this disorder, and provide novel targets for the discovery of interventions to treat and prevent this disorder. Information about the genes that are preferentially expressed in relationship to normal neurological aging could provide new information about the molecular mechanisms that are involved in normal age-related cognitive decline and a host of age-related neurological disorders, and they could provide novel targets for the discovery of interventions to mitigate some of these deleterious effects.</p>